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Can methylation deficit effect on myelin tie together ME/CFS, autism,FM, MS, and EMH?

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by richvank, Jun 7, 2011.

  1. richvank

    richvank Senior Member

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    Hi, Wally and the group.

    I have been in contact with Dr. Graham, Dr. Havas, and the webmaster of the electricalpollution.com site. I am trying to come up to speed on the EMH issue and the hypotheses that have been proposed for the mechanisms behind it. I've been invited to give a talk in Sweden in the fall, and this is one of the topics they are interested in there. I'll post about it as I get a better understanding of it. I appreciate the contacts.

    Rich
     
  2. richvank

    richvank Senior Member

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    Thanks, Lisa.

    I haven't had a chance to study the gliotoxin stuff yet. Right now I'm focusing on electromagnetic hypersensitivity and myelin. Don't know if myelin is relevant to fibro or not. There was an interesting electron microscopy paper from South Korea that reported some ballooning of Schwann cells in peripheral nerves in fibro. The Schwann cells make myelin for the peripheral nerves.

    Rich
     
  3. richvank

    richvank Senior Member

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    Hi, Dufresne.

    Thanks for the input. I have seen some reports indicating that EMH is associated with oxidative stress. That would certainly tie in with glutathione depletion. I don't know what to make of the burning skin and eyes. There's one woman in the UK who has posted pictures of her face before and after, and it is quite striking. Maybe induced currents produce oxidative stress in the skin.

    How do you know that you have peripheral demyelination? Have you had some neurological testing, such as conduction velocity?

    Rich
     
  4. richvank

    richvank Senior Member

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    Hi, Tania.

    Thanks for the information.

    The only clinical study that I know of that has been done on methylation and ME/CFS is the one that Neil Nathan, M.D., and myself did. The report is here:

    http://aboutmecfs.org.violet.arvixe.com/Trt/TrtMethylStudy09.pdf

    I don't know how "proper" you would think it was. We did what we could with the setting the funding that we had. There was no placebo control or randomization. It was open-label, not blinded. We used subjective reports of symptom severity from the patients, not objective measures of activity or fatigue, sleep, or cognition. We did do objective lab testing of methylation parameters. You will have to judge for yourself how worthwhile it was. Personally, I was very happy to see the results we got, and I think the lab tests tell a pretty good story.

    Best regards,

    Rich
     
  5. richvank

    richvank Senior Member

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    Hi, Mr. Kite.

    I think the reversed gender prevalences between ME/CFS and autism are caused by the differences in hormones. Little boys have more testosterone than little girls, and in fact there is a burst of it in utero when the sex organs are being developed in boys. There are suggestions in the literature that testosterone causes higher toxicity of mercury. Maybe that's the connection in autism. In ME/CFS, where the female gender bias occurs in the post-puberty onsets, I have suggested that it results from some people inheriting polymorphisms in CYP1B1, COMT, the GST enzymes and sometimes SOD. When this combination occurs in a woman, she will have difficulty metabolizing estrogens, and she will experience redox cycling as a result, giving her an additional bias toward oxidative stress. This adds another straw to the camel's back in terms of depleting glutathione, and that's what brings on ME/CFS in most cases, according to my hypothesis. I have several Genovations Detoxigenomic Profile reports from women who have ME/CFS, and this combination of SNPs comes up often. Men inherit them, too, but they don't have as much of the estrogens to dispose of, so it doesn't cause oxidative stress in them.

    Best regards,

    Rich
     
  6. richvank

    richvank Senior Member

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    Hi, Freddd.

    Thanks for the input on MS, Parkinson's and your response to electric blankets. It does seem as though the methylation--myelin connection may be in important part of the picture.

    Rich
     
  7. Freddd

    Freddd Senior Member

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    Hi Voner,

    I think that if you're going to delve deep into the complexities of the methylation cycle and the involvement of vit b12, then you need to delve deep into the complex cities of glial cells also. And then hook your together relationships of vitamin B12 and glial cells



    Don't forget Schwann cells.


    My one wish is that -- somehow all of both the your musings could be boiled down into a simple paragraph or in some form that I (and many others) could easily understand. But maybe that is for the future and this is still the hashing out stage.

    I don't think you understand the nature of the questions we are hashing out by the comments you are making. I'll sum it up for you in this one simple paragraph. Do you want to get busy healing your problems or debate it's simplicity or complexity while they continue to worsen until more of the damage is irreversible? I post only a few musings and try to make clear when they are musings or hypothetical or theoretical considerations or speculations. Most of what I post is pragmatically based. I can't "prove" a thing. I can demonstrate it over and over. However, if you are a betting man I might set odds and make a bet. I am certainly willing to guarantee a certain percentage of results of a certain magnitude and base 100% of my compensation on that for a selected population. In the insurance business it's called "rate-making". I'm playing "You Bet Your Life". I've placed my bets and no longer suffer most all those problems you still have.


    I USED to "have some nasty neurological symptoms allodynia, hyperalgesia, etc (a hypersensitive pain system -- including touching (ie, typing) anything causes lots of pain)", drop foot, lack of position sense, numbness of feet, neuropathic bladder, poly neuropathy, 10 different types of muscle pains, muscle atrophy, etc etc etc. I still do have some of the effects of subacute combined degeneration, about 10% of the over 200 symptoms I used to have, and those are very reduced. Everything else is long healed. The active b12 protocol as reported here and elsewhere does indeed work for correcting these things. I have done so as have many others. It isn't perfect. There are still gaps in my understanding and in the protocol. However, I can tell you how to largely heal the peripheral nervous system and stop the deterioration of the CNS and even reverse such deterioration to a large extent, but not perfectly. It's a complex problem. I'm not talking about a theoretical "this ought to work" but .... Rather I am talking about a pragmatic system that works for a sizable percentage of people trying it.

    Both the you keep referring to myelin, as if it was a simple substance. It isn't.

    Well of course it isn't. It likely is as complicated as the "b12" situation. Way back in the dark ages when I was a freshman in college and the planar transistor was only 7 years old and ICs were in their infancy, computers were just changing from core memory to solid state memory and the microprocessor was still some years away, freshman were still buying their fancy high tech Pickett slide-rules, the head of the Physics dept at WPI told the freshman class during orientation week that half of everything they were going to teach us would be superseded or proven wrong before we retired. The school had it's brand new shiny 7094 II (32K of 36 bit words in 7090) running Fortran IV on order and a 300 baud terminal to the New England Computational Facility at MIT for time sharing on their 7094. Not much has changed since then, has it? Looking at the guts of a computer these days it looks a lot simpler and has very few parts compared to even a mini-computer of those days. Appearances can be deceptive.

    Why would you think that Rich and I think that the biochemistry of myelin is simple? I realize that neither of us have written and posted any post-doc dissertations on myelin here. I am very focused on healing. 90% of that is knowing what is going on well enough so that "good" questions can be asked that can receive "good" answers. Otherwise it is GIGO all the way.

    And then hook your together relationships of vitamin B12 and glial cells

    And it has to be my understanding of b12 because the understanding of b12 used as references in myelin research is based almost entirely GIGO b12 research. In the GIGO b12 research 90% of everything they think they understand will be proven wrong in the long run because of fundamental invalid assumptions at the very foundation of most of such research. My current understanding has healed most of my neurological problems and holds the rest at bay for the time being. I won't stop improving this until I'm stumps up or my brain stops working. What I have found in the past few months now requires a complete re-thinking taking it, the new info, into account and a new trip to the literature looking for clues that were not noticeable before.
     
  8. hixxy

    hixxy Woof woof

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    In my experience EMF sensitivity tends to come and go in it's intensity, not just day to day, but even hour to hour. I can't see how this could possibly be caused by demyelination. I'm with Dufresne on the oxidative stress theory.
     
  9. richvank

    richvank Senior Member

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    Thanks, hixxy.

    It may be that both are involved. That is, myelin damage may make one more vulnerable to the effects of oxidative stress, and then the level of the oxidative stress may vary as the glutathione level varies. I have suspected that the phenomenon of "crashing" may reflect a drop in glutathione as a result of increased demand.

    Rich
     
  10. rydra_wong

    rydra_wong Guest

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    I actually have quite a lot of info on M.S. but too long to type right now. Only thing I wanted to say now is I have 18 genetic defects out of 30 tested, many in the methyl cycle. I have slow brain processing time -- always have lifelong. My father also. I think it may be pertinent that the methyl cycle in the brain is NOT LIKE the methyl cycle in the rest of the body. Specifically there is no P5P path to get rid of homocysteine and there is no TMG/betaine path to recycle the homocysteine. The brain ONLY relies on methylcobalamin plus methylfolate...NOTHING ELSE. The brain, however, is a a small percentage of the body. SO measuring total body homocysteine levels may not be indicative of neural methylation health. I think the brain could be quite off and only detected by an 'insignificant blip' in the homocysteine level.
     
  11. richvank

    richvank Senior Member

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    Hi, rydra.

    You might be interested in the study that was done by Prof. Regland and coworkers in Sweden a few years ago. The homocysteine level was found to be normal in the blood serum, but high in the spinal fluid. I think that supports what you are saying.

    Best regards,

    Rich
     
  12. globalpilot

    globalpilot Senior Member

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    DOes anyone know what is meant by the statement that the low homocysteine found implies methylation is necessary but not sufficient for myelin production ?

     
  13. rydra_wong

    rydra_wong Guest

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    I can't read all this stuff about m.s. since I don't have it but I read the first posting and did not see the things I know about m.s. so here goes for those who are interested:
    (1) on the radio about 5 years ago was reported a study that said tetanus shots confer immunity to m.s.
    (2) The web states that those with m.s. have low uric acid. uric acid is a cellular level antioxidant which appears to be very important to fending off m.s. Those with gout (my family) do not get m.s. This is an EXTREMELY INTERESTING article: http://en.wikipedia.org/wiki/Uric_acid And here is the bit about causes of low uric acid and m.s.:
    Causes of low uric acid
    Low dietary zinc intakes cause lower uric acid levels. This effect can be even more pronounced in women taking oral contraceptive medication.[34]

    Xanthine oxidase is a copper, iron, and molybdenum-containing enzyme, so people with iron deficiency (the most common cause of anemia in young women) or molybdenum deficiency can experience low uric acid
    Xanthine oxidase loses its function and gains ascorbase function when some of the Fe atoms in XO are replaced with Cu atoms. Accordingly, people with high Cu/Fe can experience low uric acid and vitamin C deficiency, resulting in oxidative damage. Since estrogen increases the half life of Cu, women with very high estrogen levels and intense blood loss during menstruation are likely to have a high Cu/Fe and present with low uric acid
    Sevelamer, a drug indicated for prevention of hyperphosphataemia in patients with chronic renal failure, can significantly reduce serum uric acid.[35]

    Multiple sclerosis
    Lower serum values of uric acid have been associated with multiple sclerosis (MS). MS patients have been found to have serum levels ~194 mol/L, with patients in relapse averaging ~160 mol/L and patients in remission averaging ~230 mol/L. Serum uric acid in healthy controls was ~290 mol/L.[36] Conversion factor: 1 mg/dL=59.48 mol/L[17]

    A 1998 study completed a statistical analysis of 20 million patient records, comparing serum uric acid values in patients with gout and patients with multiple sclerosis. Almost no overlap between the groups was found.[37]

    Uric acid has been successfully used in the treatment and prevention of the animal (murine) model of MS. A 2006 study found elevation of serum uric acid values in multiple sclerosis patients, by oral supplementation with inosine, resulted in lower relapse rates, and no adverse effects.[38]

    Normalizing low uric acid
    Correcting low or deficient zinc levels can help elevate serum uric acid.[39]
    Inosine can be used to elevate uric acid levels.[36]
    Zn inhibits Cu absorption, helping to reduce the high Cu/Fe in some people with hypouricemia.
    Fe supplements can ensure adequate Fe reserves (ferritin above 25 ng/dl), also correcting the high Cu/Fe.

    Oxidative stress
    Uric acid may be a marker of oxidative stress,[40] and may have a potential therapeutic role as an antioxidant.[41] On the other hand, like other strong reducing substances such as ascorbate, uric acid can also act as a prooxidant,[42] particularly at elevated levels. Thus, it is unclear whether elevated levels of uric acid in diseases associated with oxidative stress such as stroke and atherosclerosis are a protective response or a primary cause.[43][44]

    For example, some researchers propose hyperuricemia-induced oxidative stress is a cause of metabolic syndrome.[32][45] On the other hand, plasma uric acid levels correlate with longevity in primates and other mammals.[46] This is presumably a function of urate's antioxidant properties.[47]

    (3) I have always known that m.s. is caused by destruction of the myelin sheath and myelin is fat and so I have always reasoned that antioxidants which prevent rancidity of fat would be protective. I do not know which antioxidants work where but it is a good guess that the ones which are fat soluble are important. For instance Vitamin E is oil soluble and can cross the lipid wall of the cell. Vitamin C is water soluble and cannot. Alpha Lipoic acid is soluble in fat AND water and can work in both places. Some cellular antioxidants like apparently glutathione and uric acid are more important than these because they are there where they are needed. I think also SOD is one of those super-important anti-oxidants.

    (4) When the myelin sheath which insulates the nerve from other nearby nerves is damaged this allows "cross-talk" between the nerves which is what causes the overstimulation and pain.

    (5) Fredd says that omega-3 is needed to regenerate nerves as well as the B12 methylation supplements and this makes sense as the myelin sheath is fat.

    (6) This is the most interesting info I have learned in the past year on nerves -- it is extremely interesting. www.lef.org says that the nerve cell does not use insulin to gate sugar entry (and thereby fend it off when undesireable) like the non-nerve cell does. The normal method it is supposed to gate and fend off sugar is via carnitine. It requires adequate methylation to make carnitine. If you do not have enough carnitine, sugar gets into the nerve cell and the nerve cell cannot get rid of it and it turns to sorbitol and damages the cell. This has to do with the polyol pathway. I read this in Life EXtensions compendium book which explains it better than the online references I can find, but here they are (which I retrieve with search string "polyol pathway"):

    (p.s. I believe neuropathy is neuropathy whatever the cause so I think this applies despite that it was studied in the context of diabetes - for instance doctors in India are treating neuropathies caused by tropical diseases (chagas I believe?) with b12 therapies successfully)

    Polyol pathway hyperactivity is closely related to carnitine deficiency in the pathogenesis of diabetic neuropathy of streptozotocin-diabetic rats.

    Nakamura J, Koh N, Sakakibara F, Hamada Y, Hara T, Sasaki H, Chaya S, Komori T, Nakashima E, Naruse K, Kato K, Takeuchi N, Kasuya Y, Hotta N. The Third Department of Internal Medicine, Nagoya University School of Medicine, Nagoya, Japan.

    J Pharmacol Exp Ther 1998 Dec;287(3):897-902

    To investigate the relationship between polyol pathway hyperactivity and altered carnitine metabolism in the pathogenesis of diabetic neuropathy, the effects of an aldose reductase inhibitor, [5-(3-thienyl) tetrazol-1-yl]acetic acid (TAT), and a carnitine analog, acetyl-L-carnitine (ALC), on neural functions and biochemistry and hemodynamic factors were compared in streptozotocin-diabetic rats. Significantly delayed motor nerve conduction velocity, decreased R-R interval variation, reduced sciatic nerve blood flow and decreased erythrocyte 2, 3-diphosphoglycerate concentrations in diabetic rats were all ameliorated by treatment with TAT (administered with rat chow containing 0.05% TAT, approximately 50 mg/kg/day) or ALC (by gavage, 300 mg/kg/day) for 4 weeks. Platelet hyperaggregation activity in diabetic rats was diminished by TAT but not by ALC. TAT decreased sorbitol accumulation and prevented not only myo-inositol depletion but also free-carnitine deficiency in diabetic nerves. On the other hand, ALC also increased the myo-inositol as well as the free-carnitine content without affecting the sorbitol content. These observations suggest that there is a close relationship between increased polyol pathway activity and carnitine deficiency in the development of diabetic neuropathy and that an aldose reductase inhibitor, TAT, and a carnitine analog, ALC, have therapeutic potential for the treatment of diabetic neuropathy.

    The role of taurine in diabetes and the development of diabetic complications.
    Hansen SH. Department of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospital, Denmark. shhansen@rh.dk

    Diabetes Metab Res Rev 2001 Sep-Oct;17(5):330-46

    The ubiquitously found beta-amino acid taurine has several physiological functions, e.g. in bile acid formation, as an osmolyte by cell volume regulation, in the heart, in the retina, in the formation of N-chlorotaurine by reaction with hypochlorous acid in leucocytes, and possibly for intracellular scavenging of carbonyl groups. Some animals, such as the cat and the C57BL/6 mouse, have disturbances in taurine homeostasis. The C57BL/6 mouse strain is widely used in diabetic and atherosclerotic animal models. In diabetes, the high extracellular levels of glucose disturb the cellular osmoregulation and sorbitol is formed intracellularly due to the intracellular polyol pathway, which is suspected to be one of the key processes in the development of diabetic late complications and associated cellular dysfunctions. Intracellular accumulation of sorbitol is most likely to cause depletion of other intracellular compounds including osmolytes such as myo-inositol and taurine. When considering the clinical complications in diabetes, several links can be established between altered taurine metabolism and the development of cellular dysfunctions in diabetes which cause the clinical complications observed in diabetes, e.g. retinopathy, neuropathy, nephropathy, cardiomyopathy, platelet aggregation, endothelial dysfunction and atherosclerosis. Possible therapeutic perspectives could be a supplementation with taurine and other osmolytes and low-molecular compounds, perhaps in a combinational therapy with aldose reductase inhibitors. Copyright 2001 John Wiley & Sons, Ltd.

    Oh, here I find this is their newsletter: http://www.lef.org/newsletter/2004/2004_12_30.htm?source=search&key=polyol pathway

    One predominant theory of neuropathy in diabetic rats involves abnormalities in what is called the polyol pathway. Polyol stands for polyhydroxy alcohols. While most of the cells in the body require insulin in order to transport glucose across the cell membrane, nerve cells are different. Membranes of nerve cells and their capillaries have insulin-independent glucose transport; that is, insulin is not required for glucose to pass into the cells. Since there is an excess of glucose in the bloodstream of diabetics, this glucose can easily be absorbed into nerve cells. In nerve cells, this glucose gets converted to sorbitol (a sugar alcohol) by an enzyme known as aldose reductase. The sorbitol cannot easily get out of the cell and consequently it accumulates, causing free-radical damage to nerves and blood vessels. This causes a decrease in an intracellular nutrient known as myo-inositol that is partly responsible for nerve conduction.

    There is also an increase in free radicals such as peroxides and decreased nitric oxide production (a blood vessel-relaxing messenger), which, of course, leads to increased oxidative stress and the need for increased antioxidants. The amino acid taurine is also depleted (Hansen 2000). Terada et al. (1998) suggest that there is a close relationship between increased polyol pathway activity and carnitine deficiency in the development of diabetic neuropathy and that an aldose reductase inhibitor, a carnitine analog, and alpha-lipoic acid have therapeutic potential for the treatment of diabetic neuropathy (Terada et al. 1998).

    ---

    So y'all with m.s. may not be diabetic but I think y'all are coming at the polyol pathway problem from the other direction -- a deficiency of carnitine rather than an overabundance of glucose. That's my uneducated but firm opinion. I think the way out is this: YOU CANNOT CONTROL WHAT YOU CANNOT MEASURE. Follow whichever methylation protocol you think best for you and measure your homocysteine and your carnitine. Your homocysteine should be 6.3. EVery 3 points above that is a 35% greater risk of stroke. If your homocysteine is right, you probably have the methylation cycle working in most of your body (not necessarily the brain since the methylation cycle is GREATLY ABBREVIATED in the brain (there are no workarounds for blocked paths there!). Once you get the homocysteine right (it is $60/test) then check your carnitine. The protocol you are taking is NOT RIGHT FOR YOU if you cannot get these numbers in range, so try again. Measure and adjust - that is how you get control. All along make sure you are taking omega-3. I do not know how much - I think maybe 3 g, which to me is measly since I have to take 7-9g/day to fend off NF-kB due to allergies. You can take carnitine directly of course but it will mean you have not gotton your methylation right, which will cause other issues for you. In addition, take the steps above to raise uric acid and you can measure that too! Get yourself in the sweet spot in these measures and take oil soluble antooxidants for good measure. I think that may do the trick. If not, I think these are all key steps on the way to recovery, and maybe additional research will turn up a few more steps.

    So in case you missed it, I think m.s. may be caused by a virus in genetically sensitive or for other reason methyl compromised individuals who do not happen to have the genes and or diet that causes gout. If you make your body stronger with methylation and antioxidants the virus won't make any difference. I am not sure a tetanus shot would be a good idea if you already have m.s. I guess you could try Olive Leaf Extract and Oil of Oregano against the virus. I think we make too much of virusses instead of strengthening the organism against it. So for instance there are always weed seeds about, but if you have a healthy lawn, it crowds out the weeds.
     
  14. rydra_wong

    rydra_wong Guest

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    Sandra I think it is more common to be sensitive to whatever dye/chemical they give you before the MRI. I think they may be iodine based and many people are sensitive to iodine (like me). I would consider that first. But, yes, Rich is right. The nerves are just like electric wires in this respect...if not properly insulated (in the nerve b the myelin sheath) then there can be cross talk with any other electrical charge nearby.

    Cheerz
     
  15. alex3619

    alex3619 Senior Member

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    Hi Rydra_wong, that was an intersesting analysis. I think it raises several interesting questions too. It has long been known that ME or CFS are risk factors in developing insulin resistance, and hence by implication type 2 diabetes. I wonder if carnitine deficiency could induce neurological insulin resistance then feedback effects could cause this to spread to other tissues, eventually giving rise to type 2 diabetes (maybe we need to call it type 3?). I know of lots of skinny CFS or ME patients who have developed type 2 diabetes. Its not about obesity necessarily. The "link" to obesity is based upon both animal and human models, where obese Pima Indians were chosen as they have a high diabetes risk. Against that we have Sumo wrestlers, who are technically obese, but so far as I am aware rarely get diabetes - but then they are super fit being athletes.

    My own case history perplexes doctors. I have had transient elevated homocysteine - I was unaware of how limited the normal detox paths are in the brain, thats interesting. I technically have type 2 diabetes but aside from being overweight and having neuropathy, everything is not typical. I don't have many of the usual blood markers, it does not seem to be progressive the way diabetes is, and my neuropathy does not fit the usual profile - I think I have small fibre neuropathy, but I can't test for that in Australia. My methylation genes are normal, but I have a one haemochromatosis gene, with mildly elevated iron. My uric acid is high. I have long been aware that high uric acid inversely correlates with MS risk. I wonder if its linked to a high turnover of RNA that I suspect occurs in CFS, or if it has more to do with a compensatory mechanism for oxidative stress. It could be both.

    I have long suspected that MS and ME are closely related, and some MS experts have said over the years that while they have clear MS and ME patients, most are in between and they are not sure if its one diagnosis or the other.

    One of the problems in medical research is that too often association is mistaken for causation - if it matches a pet hypothesis it tends to be taken as confirmatory. I have long been of the suspicion that our understanding of type 2 diabetes is very wrong, that what doctors are being taught in medical school is wrong (I had several medical school tutorials when studying biochemistry). The complexity of the systems involved, plus the obvious incomplete information on biochemical pathways in the body, has led medicine down many a false path.

    Funny enough omega-6 fats are also good for helping to cope with insulin resistance, although I tend to avoid long chain omega-6s due to rapid inflammatory symptoms after eating them.

    So a question for those interested in methylation: will supporting methylation pathways in the body substantially assist carnitine levels in the brain? It migth depending on transport capacity. Low levels of carnitine are frequently found in ME and CFS. Has anyone raised serum carnitine substantially using methylation protocols?

    I strongly suspect we have a huge drain on methylation pathways due to high protein synthesis and DNA repair. It is entirely possible that normal methylation capacity is overwhelmed by ME issues resulting in a functional insufficiency of methyl donors - quite apart from the reasons usually given in methylation cycle discussions.

    Bye
    Alex
     
  16. rydra_wong

    rydra_wong Guest

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    hm. I can't quote all that - you type almost as much as I do! I have lots of broken methylation genes. But I guess I do not have ME because supposedly ME can be diagnosed with ESR and mine is fine. I did not ever measure carnitine until after being on Fredd's protocol for over a year but my carnitine is excellent. I DID measure my homocysteine before Fredd's protocol due to having diagnosed high blood pressure and it was way off, despite taking B100 every day of my life. Fredd's protocol fixed this.

    I don't think there is any feedback between m.s and diabetes. I am just saying they are different directions to take to get the same neuropathy. I do not discount at all that the same individuals get these things because improper methylation causes MANY things as methyls are used to turn on/off chemical reactions all throughout the body. It is possible that homocysteine, a neurotoxin, could do some damage to the pancreas. But I am not so sure that's it because of some things I read in Life Extension. They report on a study proving (if one single study proves anything) that Olive Leaf Extract protects the beta cells of the pancreas from damage leading to diabetes. The thing they said causes the damage is -- hang on, I will have to perform a search -- here it is:
    http://www.lef.org/magazine/mag2010/jan2010_The-Secret-Behind-The-Mediterranean-Diet_02.htm?source=search&key="olive"%20"diabetes"%20"pancreas"

    In the summer of 2009, Italian researchers published a study suggesting that olive oil polyphenols may slow or prevent the progression of type 2 diabetes.43

    They focused on amylin, a pancreatic hormone that normally works in concert with insulin to regulate blood sugar levels. However, in its abnormal formcalled a toxic peptide aggregateamylin destroys the cells in the pancreas responsible for making insulin.

    Since oleuropein is the primary phenolic component of olive oil, the Italian team focused on oleuropeins effects on amylin aggregation and toxicity. In laboratory experiments, researchers found that oleuropein, when present during the formation of the toxic amylin aggregate, consistently prevented it from destroying insulin-producing cells.43

    ---

    For some reason I think low BH4 is linked to diabetes, but I can't rememebr what I read to make me think that.

    The thing is that many people with methylation issues get that way due to genetic mutations and if you have genetic mutations, why would they just be in the methylation cycle? There is something about your MOTHER'S methylation status which has something to do with YOUR gene expression and there is also something about your OWN methylation status that has something to do with your gene expression. If you have compromised gene expression it is likely not only n one place. That is the only real tie I think there is between ms and diabetes. I cant defend it at all -- it s just my gut feeling.

    ====

    I should add in order to be of assistance that low testosterone is linked to diabetes in men and I believe they will find that low estrogen is linked to diabetes in women. I started having severe blood sugar issues as I neared menopause (say at about age 47) and I found supplements to stave it off but by age 50 nothing worked but DHEA (which is hormone replacement). I believe I would be diabetic like everyone else in my family today were it not for the DHEA.
     
  17. rydra_wong

    rydra_wong Guest

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    Transient elevated homocysteine is most likely caused by insufficient TMG. The purpose of TMG (and the BHMT pathway that uses it) is to act as a stopcock to get rid of excess homocysteine quickly after meals (it is faster than the B12/folate pathway which has multiple chemical reactions on it). People who eat diets with the most TMG get 2g/day so that is how much I take. If you take your 7-9 fruits and veggies /day that MyPyramid says you should for health then maybe you don't need it (depends on your selections of course). If like most Americans you don't even get 3 fruits and veggies/day you need to supplement this!
     
  18. rydra_wong

    rydra_wong Guest

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    Oh, you are right Alex, there is a tie. I don't know that much about that and just dont have time now to check into it but I ran across this study whcih says that methylfolate will substitute for BH4 if needs be, so there is a tie there, and looking at the biochemical pathways it looks at a glance like of course there would be a tie anyway: http://www.life-enhancement.com/article_template.asp?id=841
    Rydra
     

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